Evidence map›Paper›PMID 32236517›Full record

ArticleThe Journal of cell biology2020

Mitochondrial fragmentation enables localized signaling required for cell repair.

Adam Horn, Shreya Raavicharla, Sonna Shah, Dan Cox, Jyoti K Jaiswal

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.3field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 78 citations in OpenAlex.

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  12. ThemBio · 2024
    Article
  13. Review
  14. Article
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  16. Review
  17. C5a-C5aR1 axis controls mitochondrial fission to promote podocyte injury in lupus nephritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  18. Article
  19. Mitochondria in disease: changes in shapes and dynamics.Trends in biochemical sciences · 2024
    Review
  20. The multiple links between actin and mitochondria.Nature reviews. Molecular cell biology · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Adam HornChildren's National Health System, Center for Genetic Medicine Research, Washington, DC.
Shreya RaavicharlaChildren's National Health System, Center for Genetic Medicine Research, Washington, DC.
Sonna ShahChildren's National Health System, Center for Genetic Medicine Research, Washington, DC.
Dan CoxJohn Walton Muscular Dystrophy Research Centre, Newcastle University and Newcastle Hospitals National Health Service Foundation Trust, Newcastle upon Tyne, UK.
Jyoti K JaiswalChildren's National Health System, Center for Genetic Medicine Research, Washington, DC.
Children's National · USNational Health Service · GB

Funding

Research_ProjectU54HD090257 · NICHD · CHILDREN'S RESEARCH INSTITUTE · PI VITTORIO GALLO, VITTORIO GALLO VITTORIO GALLO · 2016 to 2020
$5.9M
Understanding the mechanism and role of cell membrane repair in Miyoshi MyopathyR01AR055686 · NIAMS · ROCKEFELLER UNIVERSITY · PI JAISWAL, JYOTI K · 2008 to 2021
$3.6M
Genetics and Genomics of Muscle Postdoctoral Training ProgramT32AR056993 · NIAMS · CHILDREN'S RESEARCH INSTITUTE · PI JAISWAL, JYOTI K, PARTRIDGE, TERENCE A · 2010 to 2019
$2.2M
NIAMS NIH HHS R01 AR055686NIAMS NIH HHS T32 AR056993NICHD NIH HHS U54 HD090257
6 · The paper itself

Abstract

Plasma membrane injury can cause lethal influx of calcium, but cells survive by mounting a polarized repair response targeted to the wound site. Mitochondrial signaling within seconds after injury enables this response. However, as mitochondria are distributed throughout the cell in an interconnected network, it is unclear how they generate a spatially restricted signal to repair the plasma membrane wound. Here we show that calcium influx and Drp1-mediated, rapid mitochondrial fission at the injury site help polarize the repair response. Fission of injury-proximal mitochondria allows for greater amplitude and duration of calcium increase in these mitochondria, allowing them to generate local redox signaling required for plasma membrane repair. Drp1 knockout cells and patient cells lacking the Drp1 adaptor protein MiD49 fail to undergo injury-triggered mitochondrial fission, preventing polarized mitochondrial calcium increase and plasma membrane repair. Although mitochondrial fission is considered to be an indicator of cell damage and death, our findings identify that mitochondrial fission generates localized signaling required for cell survival.

Indexed as

AnimalsApoptosisCalciumCalcium SignalingCell MembraneDynaminsFibroblastsHumansMiceMicrotubule-Associated ProteinsMitochondriaMitochondrial DynamicsMitochondrial ProteinsPeptide Elongation FactorsSignal TransductionCalciumDNM1L protein, humanDynaminsMicrotubule-Associated ProteinsMIEF2 protein, humanMitochondrial ProteinsPeptide Elongation Factors

Identifiers

PMID32236517
PMCPMC7199862
OpenAlexW3014671232

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.